Leukotrienes are potent pro-inflammatory mediators that are synthesized by certain bone-marrow derived granulocytes after activation (Samuelsson, Science 220:568, 1983; Lewis et al., J. Clin. Invest. 73:889, 1984). Leukotrienes have been postulated to play an important role in bronchial asthma (Margoskee, Ann. NY Acad. Sci. 629:148, 1990) and in other inflammatory diseases, such as ulcerative colitis, bronchitis, sinusitis, psoriasis, allergic and non-allergic rhinitis, lupus, and rheumatoid arthritis. 5-lipoxygenase is the first committed enzyme in the pathway leading to leukotriene synthesis and is responsible for the conversion of arachidonic acid to LTA.sub.4 via the unstable intermediate 5-hydroperoxy eicosotetraenoic acid (Samuelsson et al., Science 237:1171, 1987; Samuelsson, Science 220:568, 1983).
It has been established that treating patients with agents that have the capacity to inhibit 5-lipoxygenase results in improvement in lung function, reduction in asthma symptoms, and decreased need for alternative asthma treatments (Persson et al., Anesthesiology 82:969, 1995; Israel et al., Ann. Int. Med. 119:1059, 1993). Treatment with 5-lipoxygenase inhibitors can also benefit ulcerative colitis patients (Laursen et al., Lancet 335:683, 1990) and those suffering from rheumatoid arthritis (Weinblatt et al. J. Rheumatol. 19:1537, 1992). However, at least in the context of asthma, not all patients experience beneficial effects; there is a heterogenous response in the patient population to treatment with 5-lipoxygenase inhibitors. Prior to the present invention, the reason for this heterogeneity was not known. Moreover, there is currently no way to identify in advance those patients who will respond well, and those who will respond poorly, to 5-lipoxygenase inhibitor treatment. Accordingly, there is a need for improvements in the area of patient response. There is also a need for further analysis of 5-lipoxygenase gene regulation.